Middle cerebral artery syndromes

M1 segment

  • Contralateral hemiplegia
  • Contralateral gaze palsy, ipsilateral gaze preference
  • Contralateral hemisensory loss
  • Contralateral spatial neglect. Profound neglect in nondominant hemisphere lesions
  • Contralateral hemianopsia
  • Global aphasia if dominant hemisphere
  • Anosognosia and anosodiaphoria, confusion, whispering voice, inability to maintain eye closure, constructional apraxia may also exist at varying degrees in nondominant hemisphere lesions

M2 segment, superior division

  • Contralateral arm and face weakness
  • Contralateral gaze palsy
  • Varying degree of contralateral cortical type sensory loss in arm and face
  • Varying degree of right spatial neglect may exist in dominant hemisphere lesions. Profound left spatial neglect in nondominant hemisphere lesions
  • Broca’s (nonfluent) aphasia if dominant hemisphere

M2 segment, inferior division

  • Usually mild or no motor deficit
  • Varying degree of contralateral cortical type sensory loss in arm and face
  • Profound left spatial neglect if nondominant hemisphere
  • Wernicke’s (fluent) aphasia if dominant hemisphere
  • Contralateral superior quadrantanopia or hemianopia
  • There may be ipsilateral gaze preference at onset

Deep, penetrating (lateral lenticulostriate) branches from M1 segment

  • Contralateral hemiplegia
  • Contralateral hemisensory loss
  • Transcortical motor or sensory aphasia

Orbitofrontal artery (superior division branch)

  • Frontal syndrome with disinhibition and socially inappropriate behaviour
  • Compulsive joking (Witzelsucht of Oppenheim)
  • Continuous laughing (moria of Jastrowitz)
  • Contralateral grasping
  • Contralateral conjugate deviation of the eyes

Precentral sulcus artery (superior division branch)

  • Contralateral arm weakness
  • Contralateral limb-kinetic apraxia
  • Motor impersistence if nondominant hemisphere
  • Apraxia of eyelid closure
  • Contralateral hemineglect

Prefrontal artery (superior division branch)

  • No motor or sensory deficit
  • Cognitive and behavioral deficits including perseveration, loss of planning ability, imitation and utilization behavior, poor abstraction, abulia and apathy
  • Prefrontal syndrome of Luria - inability to follow sequential instructions, disinhibition and impulsive behavior
  • Transcortical motor aphasia may be present

Central sulcus artery (superior division branch)

  • Contralateral hemiparesis if proximal occlusion or arm weakness if more distal occlusion
  • Contralateral hemisensory loss if proximal occlusion or arm sensory loss if more distal occlusion
  • Bilateral damage to the low primary motor cortex may result in the Foix-Chavany-Marie syndrome characterised by severe dysarthria, loss of voluntary control of facial, masticatory, lingual and pharyngeal muscles with preserved reflexive and automatic functions

Postcentral sulcus artery

  • Conduction aphasia (damage to arcuate fasciculus) if on dominant hemisphere
  • Contralateral hemisensory disturbances, including allodynia and spontaneous pain resembling thalamic infarction
  • Rarely, cheiro-oral syndrome (hemisensory loss of contralateral mouth and fingers) may be observed
  • Contralateral hemineglect with possible asymbolia (inability to recognise or attach meaning) for pain
  • Minimal motor weakness in face and arm may be observed
  • Ataxia without hemisensory loss may be observed
  • Contralateral visuospatial hemineglect, especially in nondominant hemisphere lesions

Temporal arteries (inferior division branches)

(temporooccipital, posterior temporal and middle temporal arteries)

  • Wernicke’s aphasia if dominant hemisphere
  • Alexia with agraphia if dominant hemisphere
  • Contralateral visual hemineglect if nondominant hemisphere
  • Micropsia if nondominant hemisphere
  • Amusia - defect in processing pitch, musical memory and identification of tone and melody. Typically results from nondominant hemisphere lesion
  • Constructional apraxia if nondominant hemisphere
  • Confusion, hallucinations, restlessness and distractability may be observed, probably resulting from disruption of limbic structures, most often of the nondominant hemisphere
  • Acute agitated delirium has been described in infarcts of the nondominant middle temporal gyrus

Posterior parietal artery (may originate from upper or lower division)

  • Contralateral weakness in arm and face
  • Contralateral cortical sensory loss in arm and face
  • Contralateral hemiextinction on bilateral sensory stimulation
  • Ideomotor apraxia
  • Wernicke’s aphasia or anomic aphasia if dominant hemisphere
  • Constructional dyspraxia if nondominant hemisphere

Angular artery (may originate from upper or lower division)

  • Alexia with agraphia
  • Gerstmann syndrome: agraphia, acalculia, finger agnosia/anomia, left-right disorientation if dominant hemisphere, often resulting from damage to the inferior parietal lobule.
  • Bilateral infarcts can produce Bálint’s syndrome: optic apraxia (loss of voluntary control of eye movements), optic ataxia, asimultagnosia (inability to direct a panoramic view) and visual inattention.